Overnight dehydration increases the risk of a morning infarct

Simon N. Thornton, Professor

University Henri Poincare

Dear Sir,
It was with great interest that I read the recent article by A. Suarez-
Barrientos and colleagues (1). However, I think there is one very
important aspect left out of this very good clinical investigation and
that is blood volume. One of the principal problems of heart pumping is
having enough blood volume to do this with. If there is insufficient
volume then the heart has to alter its rate of contraction, which can
change filling time, or the force of contraction, which will depend on the
overall peripheral resistance and the viscosity of the blood which will
increase rates of cardiac hypertrophy and remodelling. It would appear
then to be a problem of physiological fluid (haemo-) dynamics.

In the study reported here the authors wrote that "the infarct size
was found to be significantly larger with STEMI onset in the dark-to-light
transition period (6:00 to noon)". This is the first section of the day
after an overnight period of sleep. Fluid consumption is not usually
recommended during this period yet there is substantial loss of water
which leads to overnight dehydration of both the intra and extracellular
compartments (2). Therefore, at the end of the sleep period there would be
an overall decreased blood volume, which would imply reduced perfusion
throughout the vascular system, with perhaps an increase in viscosity, and
thus extra work for the heart. It would therefore not be surprising to see
an increased number of infarcts occuring in this period.
One of the indicators of insufficient blood volume is an increase in
plasma levels of the hormones making up the renin-angiotensin-aldosterone
system (RAS) (3). Although none of these hormones are treated in the
current article I imagine if they were measured they would be increased in
the period 6.00 to noon. Furthermore, antagonists of the RAS are used
extensively in the treatment of heart failure (4).
It could be suggested therefore that one way to reduce the risk of
myocardial infarction in the morning would be improved tissue perfusion
through increased water intake, perhaps before going to bed and at
intervals during sleep.

Conflict of Interest:

CIRCADIAN VARIATIONS AND MELATONIN IN THE ACUTE MYOCARDIAL INFARCTION: STILL A FORGOTTEN EXTRACARDIAC FACTOR.

Alberto Dominguez-Rodriguez, Clinical Research

Pedro Abreu-Gonzalez

Hospital Universitario de Canarias

To the Editor:

We read with great interest the article by Su?rez-Barrientos et al
(1) regarding circadian oscillations on infarct size. Although the article
is both exhaustive and clinically relevant, we felt that the authors
failed in the recognition of the potential value of melatonin in the
association between cardiovascular events and circadian variation.

Synchrony between external and internal circadian rhythms and harmony
among molecular fluctuations within cells are essential for normal organ
biology. Circadian clocks exist within multiple components of the
cardiovascular system. These clocks have the potential of affecting
multiple cellular processes and, therefore, they hold the promise of
modulating various aspects of cardiovascular function over the course the
24-hr cycle (2). Many aspects of cardiovascular physiology are subject to
diurnal variations, and serious adverse cardiovascular events appear to be
conditioned by the time of day. The internal oscillator, or control
station regulating the body's circadian clock, is the suprachiasmatic
nucleus, a tiny structure located in the hypothalamus above the optic
chiasm. The circadian pacemaker within the suprachiasmatic nucleus
stimulates the pineal gland to produce circadian melatonin with high serum
levels during the night (2). The results of many publications suggest a
decrease in circulating melatonin concentration at different stages of the
coronary heart disease in humans. Furthermore, experimental and clinical
data suggest that melatonin is involved in normal cardiovascular
physiology (3).

Melatonin is known to be a powerful radical scavenger of the hydroxyl
radical and to protect against cardiac tissue damage mediated by oxidative
stress (2). A recent study from our group showed, in patients with ST-
elevation myocardial infarction undergoing primary percutaneous coronary
intervention, a relationship between melatonin concentrations and ischemia
-modified albumin, a marker of myocardial ischemia. Our data suggest that
melatonin acts as a potent antioxidant agent, reducing myocardial damage
induced by ischemia/reperfusion (4). Furthermore, melatonin rhythmicity
appears to have crucial roles in various cardiovascular functions as an
antioxidant, an anti-inflammatory agent chronobiotic and possibly as an
epigenetic regulator (2).

We recognize that melatonin is of special interest, beging an
endogenous molecule that can be used in humans, and which is also safe.
The omission in the articles, such as that of Suarez-Barrientos et al (1),
could deprive at the medical community of potentially useful information.